Distribution of 25-hydroxycholesterol in plasma lipoproteins and its role in atherogenesis. A study in squirrel monkeys.

@article{Peng1982DistributionO2,
  title={Distribution of 25-hydroxycholesterol in plasma lipoproteins and its role in atherogenesis. A study in squirrel monkeys.},
  author={S. Peng and C. B. Taylor and E. Mosbach and W. Y. Huang and J. Hill and B. Mikkelson},
  journal={Atherosclerosis},
  year={1982},
  volume={41 2-3},
  pages={
          395-402
        }
}
Oxidation products of cholesterol have been shown to be potent inhibitors of cholesterol biosynthesis and also highly toxic to cultured aortic smooth muscle cells. In rabbit experiments, these compounds produced arterial injury resulting in arteriosclerosis. Purified cholesterol only minimally inhibited cholesterol biosynthesis and had no effect on cultured aortic smooth muscle cells. This raises the possibility that plasma lipoproteins containing beta-apoprotein (i.e. LDL and VLDL), which are… Expand
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Radioactivities of each fraction in lipoproteins separated by thin layer chromatography showed that fractions containing cholestane-3 beta,5 alpha,6 beta-triol, 7 alpha- and 7 beta-hydroxycholesterol and 7-ketocholesterol were more selectively transported in VLDL, whereas most of the 25-hydxycholesterol was present in LDL, while HDL contained only minute amounts of cholesterol oxidation products. Expand
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TLDR
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Comparative atherogenic effects of cholesterol and cholesterol oxides.
TLDR
Oxidized cholesterols in the concentrations and relative compositions administered here are markedly less atherogenic to rabbits than highly purified cholesterol. Expand
Cholesterol oxidation derivatives and arterial endothelial damage.
TLDR
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Purified cholesterol showed no cytotoxic effect and minimal inhibition of cholesterol biosynthesis, while autooxidation products of cholesterol has the capability of inducing rabbits' aortic smooth cell death in vitro. Expand
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The results showed that 25-hydroxycholesterol and cholestane-3beta, 5alpha, 6beta-triol were probably responsible for the biological toxicity of the concentrate, whereas purified cholesterol at the same concentration produced no toxic effects. Expand
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The rate of inhibitioin due to 25-hydroxychelecalciferol is considerably greater than that of the oxygenated cholesterol analogs, and this indicates that cholesterol biosynthesis in vitro by normal and leukenic guinea pig lymphocytes is inhibited. Expand
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The data indicate that during the formation of the intermediate lipoprotein all lipid and apoprotein components other than apop protein B leave the density range of VLDL to a varying degree, and whether these same changes occur during the clearance of V LDL in vivo is yet to be established. Expand
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Observations suggest that concomitant with continuous triglyceride hydrolysis, apoLP-glu and apo LP-ala leave the very low density lipoprotein density range resulting in molecules relatively poor in triglyceride and relatively rich in apoLDL. Expand
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It is raised that a prerequisite for the regulation of cholestero-genesis in cultured fibroblasts is the initial binding of low density lipoproteins to the high affinity surface receptor sites and that a defect in this process represents the primary genetic abnormality in the disorder familial hypercholesterolemia. Expand
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A possible role for a cell surface receptor that binds plasma low density lipoproteins and regulates the sterol content of cells by modulating the rates of uptake, esterification, and synthesis of cholesterol is discussed. Expand
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The inhibitory sterols caused a similar but slower decline in the concentrations of unesterified and total cholesterol in fetal mouse liver cell cultures and rat hepatoma cell cultures. Expand
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